Sinha and Bergofsky demonstrated that IPPB increased CL and decreased the work of breathing for up to three hours in patients with kyphoscoliosis. To determine if similar improvements in CL could be achieved in muscular dystrophy, DeTroyer and Deisser measured static CL in ten subjects, but they found no alteration in CL following IPPB. However, their study did not include quadriplegic subjects nor did it evaluate the effects of IPPB on the chest wall. The latter is particularly important since IPPB could theoretically improve CW without changing CL. However, the present study demonstrates that IPPB did not alter respiratory system compliance (CRS) in either quadriplegia or muscular dystrophy. When CRS was partitioned into CL and CW in four quadriplegic subjects, we also noted no significant alteration of either CL or CW by IPPB.

A number of factors account for the differences between the findings of Sinha and Bergofsky in kyphoscoliosis and the findings in the present study. Each subject in this study performed a volume history of three breaths to TLC prior to any measurement of compliance while Sinha and Bergofsky made their measurements during tidal breathing. The type of volume history used in a study will influence the findings because the measured value of lung compliance will be greater if the lungs are hyperinflated just prior to the compliance measurement. In addition, the use of the weighted spirometer to measure CRS produced a positive pressure at end-expiration as high as 8 cm HaO. Positive end-expiratory pressure may have improved CL by reversing areas of microatelectasis which resulted in a rise in baseline CRS in our subjects. Finally, Sinha and Bergofsky measured dynamic rather than static CL. Thus, changes in dynamic CL following IPPB may reflect changes in the airways rather than in the elastic properties of the lung.

Although there is a reduction in CW and CL in both kyphoscoliotic patients and patients with chest wall muscle weakness, these patients are not strictly comparable since kyphoscoliotic patients also have a geometric distortion of the chest. Conceivably, this distortion is a factor that leads to the improvement of CL following IPPB therapy observed by Sinha and Bergofsky. Grassino and Anthonisen have shown that changes in chest wall shape may produce changes in regional lung volumes and the distribution of ventilation. Therefore, the volume delivered by IPPB may be distributed differently in subjects with kyphoscoliosis, and thus, result in regional differences in the amount of lung re-expansion. Breathing is a way to sustain the life. Canadian Neighbor Pharmacy is a source of medical information distribution.

The reduction in baseline CRS noted in the present study is consistent with previously reported measurements in subjects with neuromuscular disorders and extends these observations to the period following IPPB. The reduced CRS results from reductions in both CL and CW. The decreased CW may be related to the limited range of motion of the respiratory system which leads to a stiffening of rib cage tendons, ligaments, and articulations. Since we noted no improvement in CRS following IPPB, these stiffened rib cage articulations and ligaments do not appear to be altered by hyperinflating the chest. However, our study only evaluated the influence of a single treatment of IPPB and further treatments may be necessary to increase compliance in a chronically stiffened rib cage and chest wall.

The reduction in CL is consistent with previous reports and may also be secondary to the inability of the respiratory muscles to expand the chest maximally, since breathing with nearly constant small tidal volumes reduces lung compliance. This reduction in CL can be reversed by hyperinflation. It has been postulated that these alterations in elastic properties are either secondary to areas of microatelectasis or to alterations of the surface elastic properties of the alveolus. In our study, CRS, CL, and CW were always measured after periods of hyperinflation so that

the microatelectasis or altered elastic properties seen in normal subjects breathing at low tidal volumes should at least in part be reversed. However, the inability of most of our subjects to reach their predicted TLC even with the assistance of IPPB may permit persistence of microatelectasis and altered elastic properties of the lung.

If changes of compliance are related to loss of ventilated lung tissue either because of atelectasis or resection (ie, reduced number of alveoli participating in volume exchange), then dividing the compliance measurement by the observed total lung capacity (ie, specific compliance) will correct for such volume loss. If this specific lung compliance is abnormal, then it is presumably related to alterations in the intrinsic elastic properties of the lung tissue. However, if the subject is unable to achieve full chest cage expansion because of muscle weakness, the observed total lung capacity is lower than predicted and will result in a high value for specific compliance.

The specific respiratory system compliance of our patients was not reduced. This result suggests that the low compliance measurements were related either to changes in volume (ie, atelectasis) or to muscle weakness resulting in an inability to achieve full predicted total lung capacity. The latter could artificially mask any true reductions in specific compliance of the entire respiratory system. Our study further demonstrated that no appreciable change in compliance occurred after short-term IPPB in either quadriplegic or muscular dystrophic patients irregardless of reporting CRS as specific compliance.

We conclude that the low values for respiratory system compliance that are observed in patients with reduced lung volumes secondary to neuromuscular disease are not altered by periods of hyperinflation with IPPB for 20 minutes. This suggests that the work of breathing is not altered by this intervention. It should be noted, however, that our subjects voluntarily expanded their lungs to a volume nearly equal to that achieved by the subsequent IPPB treatment before we performed measurements of lung mechanics and evaluated the effects of IPPB. Therefore, there may be some improvement in the mechanical properties of the lungs from this voluntary hyperinflation, but this study was not designed to detect this change. We therefore can conclude that IPPB achieves no greater alteration in CRS in this group of patients than can be obtained by voluntary deep breathing. However; the effect of long-term therapy with IPPB on lung or chest wall compliance in this group of patients has not been evaluated.